Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA297957 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Graft versus host disease (GVHD) is the most common complication of hematopoietic stem cell transplant (HCT). However, our understanding of the molecular pathways that cause this disease remains incomplete, leading to inadequate treatment strategies. To address this, we measured the gene expression profile of non-human primate (NHP) T cells during acute GVHD (GSE73723). Within these profiles we discovered potentially druggable targets not previously implicated in GVHD, prominently including aurora kinase A (AURKA). In this study, we performed a planned comparison of AURKA gene expression in HCT-recipients with clinical GVHD and compared it to expression in HCT-recipients without clinical GVHD.
2015-11-29 | GSE73809 | GEO
Project description:Biologic markers of immune tolerance may facilitate tailoring of immune suppression duration after allogeneic hematopoietic cell transplantation (HCT). In a cross-sectional study, peripheral blood samples were obtained from tolerant (n=15, median 38.5 months post-HCT) and non-tolerant (n=17, median 39.5 post-HCT) HCT recipients and healthy control subjects (n=10) for analysis of immune cell subsets and differential gene expression. There were no significant differences in immune subsets across groups. We identified 281 probe sets unique to the tolerant (TOL) group and 122 for non-tolerant (non-TOL). These were enriched for process networks including NK cell cytotoxicity, antigen presentation, lymphocyte proliferation, and cell cycle and apoptosis. Differential gene expression was enriched for CD56, CD66, and CD14 human lineage-specific gene expression. Differential expression of 20 probe sets between groups was sufficient to develop a classifier with > 90% accuracy, correctly classifying 14/15 TOL cases and 15/17 non-TOL cases. These data suggest that differential gene expression can be utilized to accurately classify tolerant patients following HCT. Prospective investigation of immune tolerance biologic markers is warranted. Samples were collected after allogeneic hematopoietic cell transplantation (HCT) or in healthy control subjects. Peripheral blood samples were obtained from tolerant (n=15, median 38.5 months post-HCT) and non-tolerant (n=17, median 39.5 post-HCT) HCT recipients and healthy control subjects (n=10).
2015-05-25 | E-GEOD-64300 | biostudies-arrayexpress
Project description:RNA extracted at 240min. Samples are rRNA depleted. Expression measurement of Homo sapiens genes.
2019-07-31 | GSE114179 | GEO
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
2010-09-25 | GSE24338 | GEO
Project description:Biologic markers of immune tolerance may facilitate tailoring of immune suppression duration after allogeneic hematopoietic cell transplantation (HCT). In a cross-sectional study, peripheral blood samples were obtained from tolerant (n=15, median 38.5 months post-HCT) and non-tolerant (n=17, median 39.5 post-HCT) HCT recipients and healthy control subjects (n=10) for analysis of immune cell subsets and differential gene expression. There were no significant differences in immune subsets across groups. We identified 281 probe sets unique to the tolerant (TOL) group and 122 for non-tolerant (non-TOL). These were enriched for process networks including NK cell cytotoxicity, antigen presentation, lymphocyte proliferation, and cell cycle and apoptosis. Differential gene expression was enriched for CD56, CD66, and CD14 human lineage-specific gene expression. Differential expression of 20 probe sets between groups was sufficient to develop a classifier with > 90% accuracy, correctly classifying 14/15 TOL cases and 15/17 non-TOL cases. These data suggest that differential gene expression can be utilized to accurately classify tolerant patients following HCT. Prospective investigation of immune tolerance biologic markers is warranted.
2015-05-25 | GSE64300 | GEO
Project description: Not available
| S-EPMC2531291 | biostudies-literature
Project description:Longitudinal Study of Immune Mediated Disorders after Allogeneic HCT Protocol (Immune Mediated Disorders after Allo-HCT) - cGVHD 6501
| PRJNA378820 | ENA
Project description:Transcriptional profiling of human mesenchymal stem cells comparing normoxic MSCs cells with hypoxic MSCs cells. Hypoxia may inhibit senescence of MSCs during expansion. Goal was to determine the effects of hypoxia on global MSCs gene expression.
2011-02-19 | GSE20463 | GEO
Project description: Not available
| S-EPMC5738339 | biostudies-literature
Project description:Acute graft-versus-host disease (GVHD) arises from dysregulated donor T cell mediated immune interactions against the host, following allogeneic hematopoietic cell transplantation (allo-HCT). However, mechanisms via which non-hematopoietic host tissues actively shape post-transplant outcomes remains incompletely defined. Here, we identify endothelial cell (EC)-intrinsic interferon-g (IFNg)—IRF1 signaling as a key pathway controlling vascular remodeling and immune tolerance after allo-HCT. Using single cell RNA sequencing of liver ECs from syngeneic and allogeneic transplant recipients, we reveal that liver ECs undergo rapid, subset-specific transcriptional reprogramming after allo-HCT, marked by strong induction of IFNg-responsive pathways. We show IRF1 is a key upstream regulator, linking IFNg signaling to endothelial activation and functional remodeling. Both in vitro and in vivo studies reveal that endothelial intrinsic IFNg—IRF1 signaling is dispensable for Th1 differentiation but required for endothelial-driven Treg expansion. Loss of endothelial IRF1 in vivo uncouples vascular integrity from endothelial-mediated tolerance, reducing endothelial activation and apoptosis but exacerbating GVHD due to impaired Treg induction. Our findings suggest that therapeutic strategies that preserve endothelial IRF1-dependent tolerogenic programs may reduce GVHD severity while maintaining protective alloimmune responses.
2026-07-13 | GSE317430 | GEO